REVIEW ARTICLE

Drugs & Aging 2000 Oct; 17 (4): 295-302 1170-229X/00/0010-0295/$20.00/0 Adis International Limited. All rights reserved.

Conceptualisation and Measurement of Frailty in Elderly People

Kenneth Rockwood,1 David B. Hogan2 and Chris MacKnight1
1 Division of Geriatric Medicine, Dalhousie University, Halifax, Nova Scotia, Canada 2 Division of Geriatric Medicine, University of Calgary, Calgary, Alberta, Canada

Contents
Abstract . . . . . . 1. Frailty and Aging . . 2. Frailty and Disability 3. Defining Frailty . . . 4. Measures of Frailty . 5. Critique . . . . . . 6. Conclusion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 295 296 297 298 299 300 301

Abstract

The use of the term frailty has shown tremendous growth in the last 15 years, but this has not been accompanied by a widely accepted definition, let alone agreed-upon measures. In this paper, we review approaches to the definition and measurement of frailty and discuss the relationship between frailty, aging and disability. Two trends are evident in definitions, which often trade off comprehensiveness for precision: frailty can be seen as being synonymous with a singlesystem problem or as a multisystem problem. The essential feature of frailty is the notion of risk due to instability (itself suggesting a balance of many factors), and has been only poorly measured to date. Future models of frailty should incorporate more precise operationalisation of the probability of frailty and better explain the relationship between disease, disability and frailty.

Elderly people have a variety of healthcare needs, which are pressing on every healthcare system worldwide. Summarising needs is a helpful prelude to devising, implementing and evaluating responses. Often, what makes the needs of elderly people particular is their multiplicity, and a blurring between problems otherwise easily characterised as medical or social. In this context, the construct of frailty has been proposed as a way to better understand the health needs of elderly people. Frailty is a term that has enjoyed substantial growth since the 1980s, but it often remains undefined.[1,2] Even when defined, it is evident that

different authors emphasise different aspects of frailty. As reviewed elsewhere,[3] the notion of frailty has included the notions of: being dependent on others being at a substantial risk of dependency and other adverse health outcomes experiencing the loss of physiological reserves experiencing uncoupling from the environment[4] having many chronic illnesses having complex medical and psychosocial problems having atypical disease presentations

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being able to benefit from specialised geriatric programmes most simply, experiencing accelerated aging. In this paper, we review these essential features of current definitions of frailty, and focus on practical considerations in its measurement for research studies. We specifically consider the relationships between frailty and disability. Finally, we also attempt to suggest important topics for future research on modelling frailty. Before we explore the particulars of frailty, its definitions and measurements, it is helpful to consider some points that can guide the discussion. At their most general level, definitions and measurements can be viewed as models. Models exist chiefly to organise and summarise existing data, and to provide a framework for the discovery and integration of new knowledge. The development of a model is itself motivated by goals, so that the evaluation of a model depends on the purpose for which it is intended. In general, however, better models achieve a high level of summary while retaining comprehensiveness and precision. The former is largely guided by theory, the latter by instrumentation. The assessment of the validity of an instrument traditionally consists of 3 aspects:[5] (i) content validity, assessed by comparing the areas specified in the measure with those of the underlying model; (ii) construct validity, assessed by the extent of correlation with like measures (convergent construct validity) and unlike measures (divergent construct validity); (iii) criterion validity, assessed by comparison to a referent (gold standard) or by the ability to predict relevant and non-arbitrary outcomes (predictive validity). Clearly, with regard to frailty, comparison to a referent is not possible.
1. Frailty and Aging The comparative vagueness of frailty and its definition is a powerful clue that the task of its modelling is not an easy one. In such circumstances, it is sometimes helpful to work by analogy and
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comparison. Recognising this, we begin by considering the relationship between frailty and aging. Inasmuch as biological organisms do not live forever, at its most basic aging can be considered as what happens to an organism with the passage of time. This is hardly satisfactory however, given that there is variability in the rates of the expression of age-related phenomena, most evident perhaps in various longevity mutant gene experiments.[6] Although the definition of aging has itself proved controversial, there is a long history considering the increase in the vulnerability of an organism over time, so that aging can be conveniently summarised as an increase in the risk of death.[7] It is evident, however, that not all deaths are preceded by frailty. At a young age, accidental death can be preceded by extreme fitness. At advanced ages, the relationship between frailty and aging is more complex. Several factors must be considered. First, as Vaupel et al.[8] have noted, there is an increase in the survivorship (i.e. a decrease in the mortality rate) at advanced ages. For example, in advanced societies the death rate for women aged 80 to 89 years has fallen by about half in the years 1950 to 1995. Secondly, as also noted by this group, at advanced ages the rate of mortality decelerates, and at very advanced ages even declines. The notion of aging (at least as measured chronologically) as an increasing risk of death must be revised. Vaupel and others[9] have for some time proposed that heterogeneity in frailty can account for the apparent deceleration in the rate of death at advanced ages without an undue fundamental threat to the relationship between aging and the likelihood of dying. Consider that frailty is equated with an increased risk of death. Any population can be made up of constituents with different intrinsic frailty profiles. As the population ages, the most frail die first, leaving groups who, of course, do not ultimately escape death, but whose mortality rates are lower. With those who have higher mortality rates dying first, the survivors proportionately have lower mortality rates. In consequence, the relentless increases in the rate of death with age weaken,
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so that the rate of increase in the mortality rate lessens with age. Indeed, at an extreme old age, virtually the only survivors are those with the lowest mortality rate, so that the rate appears even to have declined.[9] By this view, frailty is equated to an increased risk of death, and is associated with age. Although it can readily be conceded that frailty is associated with an increased risk of death, it does not follow that everything that results in an increased risk of death equals frailty. For example, the transient increase in the risk of death for adolescent males is not evidence of an increased rate of aging. Another challenge to be addressed is that, like disease and aging rates, vulnerability is not evenly distributed throughout the population. At any given age, the heterogeneity in health outcomes of a group of individuals reflects both their variable frailty profiles and variability in other factors that predispose to poor health. This perspective on frailty has been demonstrated by retrospective modelling,[8,9] but its prospective demonstration has proved elusive. This conceptualisation nevertheless yields important insights: (i) frailty represents increased vulnerability; (ii) it is heterogeneous; and (iii) it is associated with chronological aging. In effect, it becomes biological, as opposed to chronological, age. The consequences for measurement are evident, but the practical application in a single measurement remains to be defined. 2. Frailty and Disability We will continue for the moment to avoid a definition of frailty, except to consider the 3 features (vulnerability, heterogeneity and association with chronological aging) noted in section 1. The definition of disability is somewhat better understood and accepted, though not without controversies of its own.[10] The World Health Organizations construct of impairment, disability and handicap is a good starting point. An impairment generally is accepted to be an anatomical or physiological abnormality at the level of the organ system. Impairments, which give rise to functional limitations, are
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what define disability. Social impediments to the adaptation to disability result in handicap.[10] It is evident that disability and frailty share a number of similarities.[1,3,4,11-13] Each compromises function, is associated with dependency and confers an increased risk of death. Each is more common with advancing age. Two factors chiefly differentiate disability from frailty. The first is the cause: disability can arise from dysfunction of a single system or from many systems, but frailty always means multisystem dysfunction. In addition, disability need not be associated with instability, whereas frailty necessarily is. By instability, we mean that small changes in input can lead to disproportionately large effects, events modelled by nonlinear dynamics. It is perhaps useful to contrast this notion of stability with a similar, but discrete, notion of consistency. Stable systems are consistent ones, but unstable systems can equally be consistent if they are not perturbed. Given, however, that unstable systems are unlikely to remain unchanged, it is necessary to also introduce the notion of dynamics, or change over time.[4,14,15] In addition, disability is a concept largely rooted within the abilities of the individual, whereas it has been proposed that the notion of frailty should be expanded to include the environmental and social context of the individual,[3,4,12,16] i.e. that frailty can be recognised at the level of the predicament, and not just the person.[13] It must be recognised, however, that the discussion about frailty and disability is not readily separable from that about frailty and aging. At some advanced age, it is unlikely that disability occurs as a single-system process, and less likely still that it does not result in an increase in vulnerability and also instability. In other words, at some age disability is a highly sensitive measure of frailty. The challenge is in the specificity. Frailty (understood as instability giving increasing vulnerability) is present in clinically important proportions of elderly people without apparent disability the socalled subclinical disability[17] or age-associated multisystem impairment.
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3. Defining Frailty Against this background, we can consider that any definition of frailty must include the following: multisystem impairment instability change over time an allowance for heterogeneity within a population[18] an association with aging[8] an association with an increased risk of adverse outcomes.[19] We will use these as criteria to consider papers in which a definition of frailty has been formally proposed, and from these definitions explore the measurement of frailty. One definition of frailty that fits the above criteria is that of Rockwood et al.,[3] initially proposed in 1994. The definition was conceptualised in terms of a balance beam. To the extent that assets and deficits were countered, frailty could be defined. Patients whose assets clearly outweighed deficits were well; those in whom the balance was precarious, or tilted in favour of deficits, were frail. Heterogeneity could be appreciated by the degree of imbalance, the process of balance changed over time and was thus dynamic, and instability was implied in that, depending on the state of the assets, a single deficit might or might not give rise to imbalance. The assets and deficits were individually associated with adverse health outcomes, and by their number and nature were multifactorial. A subsequent empirical test of the model further confirmed the multifactorial nature of the construct, and its relationship to an adverse outcome (in that instance, institutionalisation).[18] In neither the initial paper,[3] however, nor in its subsequent test,[19] was the model well enough specified to allow the description of a frailty measure to be defined readily. Another definition of frailty, proposed by Campbell and Buchner,[1] considered that frailty arises from a decline in the reserve of multiple systems, which places the frail older person at risk for disability or death with minor stresses, a notion
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they call unstable disability. This conceptualisation is clearly similar to notions of homeostenosis,[20] homeostatic disturbance[21] and functional homeostasis.[22] Campbell and Buchner also discuss the need to identify essential capacities for interaction with the environment, and the concept of system reserves. This concept of unstable disability too is multifactorial, dynamic and related to adverse health outcomes. Instability was not precisely defined by these authors, however, and an operational measure based on this definition has not appeared. As noted, a number of authors have equated frailty with disability, or with single-system dysfunction. More recently, however, there has been a move to look more systematically at the mechanisms of frailty, and this has resulted in new proposals. For example, Hammerman[23] describes clinical correlates and biological underpinnings of frailty, and holds that frailty arises from an altered metabolic balance manifested by cytokine overexpression and hormonal decline. In consequence, he is hopeful of a serum marker that can identify frailty, and serve as both a measure and a starting point for future therapeutic interventions. Interestingly, high serum interleukin-6 levels have recently been reported to predict future disability in elderly people,[24] a finding supportive of Hammermans approach. Other similar approaches view states analogous to frailty as arising from somatic mitochondrial DNA mutations (perhaps as a result of oxidative damage) accumulating in postmitotic cells and leading to senescence.[25] Similarly, frailty has been linked to low testosterone,[26] low cholesterol[27] and low dehydroepiandrosterone sulfate levels.[28] Nevertheless, this type of an approach is fundamentally different from a view that sees frailty as an emergent property of the interaction between systems which, by diverse pathways, have come to an, often subclinical, near-failure threshold.[3,12,17,24,29] In this regard it may be helpful to consider the distinction between 2 conceptual approaches to the diagnosis of any disordered state. As reviewed by Scadding,[30] definitions are conDrugs & Aging 2000 Oct; 17 (4)

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ceptually irreconcilable when approached from 2 differing perspectives, known to philosophers as essentialism and nominalism. The Hammerman approach is an essentialist one, whereas the approach proposed in this paper is nominalist, in seeing no existence of frailty apart from the patients with frailty. In a nominalist approach a phenomenon can be described, and its implications explored, in the absence of a mechanistic understanding, although one might eventually emerge. When the essentialist approach allows for a mechanistic understanding, the effect is transformative. For example, anaemia is no longer fatigue, pallor and tachycardia, but a low haemoglobin level. Where the mechanistic understanding perfectly maps the disease state, it is preferable, but it is not inherently so. Moreover, there is reason to be suspicious of the reductionist approach in explaining individual states arising from the interaction of complex systems.[31-33] The nominalist approach is not incompatible with measurement, as we will see later. 4. Measures of Frailty In considering frailty, there is a need to look at both whole person functioning and physiology so that together they provide a more complete picture of this complex disorder. Proceeding from the nominalist approach, we will consider some complementary examples of whole person measures of frailty. Our group has published a brief clinical classification of frailty which combined a selfreported measure of disability with test performance measures of cognitive impairment.[34] The rationale for this approach was to combine impairment and disability measures, and to have a measure that could readily be incorporated into routine clinical practice. The resulting measures show grades of frailty from none, to urinary incontinence only, to mild and moderate/severe. The measure is brief and easy to use, and predicts adverse health outcomes, with an evident dose-response relationship [e.g. the relative risk of institutionalisation increases from 1.0 (referent), where no cognitive
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or functional impairment is present, to 9.4 for the most frail]. On the other hand, the construct validity of the measure has not been published, and the model remains incompletely specified, with several individual factors of importance to adverse health outcomes (e.g. poor self-rated health) not specified. In addition, it does not operationalise instability or incorporate features in the individuals environment, and does not differentiate between degrees of risk in those without disability or cognitive impairment. Although not proposed specifically as a measure of frailty, the notion of allostatic load shares much with a conceptualisation of frailty that stresses the importance of the dynamic interaction between systems approaching failure. McEwen and Stellar[35] defined allostasis as the ability of the body to increase or decrease vital functions to a new steady state or challenge. In considering its content validity, we note that this approach also shares much with homeostasis, with the additional realisation that the interacting factors do not remain static. Allostatic load, therefore, becomes the cumulative wear and tear that occurs in an organism over time in the effort to maintain a steady state. But it is recognised that individual components will not wear and tear at the same rate within or between individuals. Nevertheless, it is proposed that frailty can be graded by summing across a wide range of measures that point to stress and adaptation. The measures combine several attributes, not all of which have been clearly related to the model. Some are stress indicators [e.g. cortisol excretion, noradrenaline (norepinephrine)/adrenaline (epinephrine) excretion] whereas others are markers of actual or potential diseases (blood pressure, waist-hip ratio, high density lipoprotein/total cholesterol levels and glycosylated haemoglobin levels). The measures were combined together into a scale by counting the number of instances in which an individual had lower quartile scores.[36] The predictive validity of the allostatic load measures was then tested and confirmed by examining the relationship between the load score and incident cardiovascular disease and disDrugs & Aging 2000 Oct; 17 (4)

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ability. Interestingly, and in keeping with the view that individual pathways to frailty are variable, the model was indifferent to which combination of low quartile scores gave rise to the overall pattern of allostatic load. Again considering the content validity of this approach as a measurement of frailty, it gives rise to the hypothesis that frail individuals have a narrower than normal allostatic window and have, even in a basal state, problems in keeping systems in balance. This might be reflected by the findings of Gill et al.[37] or Jarrett et al.,[38] which noted that, amongst the frail, so-called atypical disease presentations were more common. These presentations (falls, delirium and immobility) reflect failure to integrate the multiple systems needed to maintain higher order states. The allostatic load approach, with its inclusion of neuroendocrine measures, appears to be consistent with the proposed neuroendocrine-immune mechanisms for frailty.[39] Additional data are needed before the validity of this measurement approach can be incorporated into the frailty construct. In addition, the measurement of allostatic load is inherently more timeconsuming and expensive than simpler measures, which is likely to limit its widespread use. A third whole body approach to the measurement of frailty is that of Campbell and Buchner.[1] They suggest a combination of physical performance measures (grip strength, chair stand, submaximal treadmill, 8-minute walk, static balance test) and other quantitative assessments (MiniMental State Examination, body mass index, arm muscle area). How they are to be combined was left unspecified and untested. The MacArthur studies of successful aging have incorporated whole body health measures which grade risk based on performance impairment, and which might be used in conjunction with disability measures.[40] Briefly, 5 measures of physical performance (balance, gait, chair stands, foot taps and signature) in a high-functioning elderly cohort were combined into a summary score. The score was found to be predictive of subsequent decline,
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suggesting that even mild impairment can put individuals at risk for subsequent decline. Although physical performance measures have importantly added to the instrumentation armamentarium in epidemiological and clinical studies of elderly people,[41] they often prove infeasible in people with more than mild degrees of disability.[42,43] Inasmuch as they seem most useful prior to the onset of disability, and given that, at certain ages, disability is a nonspecific indicator of frailty, physical performance measures may have a particularly important role in the detection of incipient frailty at older ages. 5. Critique Clearly, no perfect measure of frailty has been developed. No measure can yet claim to have comprehensively operationalised a systematic model of frailty. No measure has yet incorporated change into its scale, even though the way in which a state was achieved or even the time course to achieve it can be as important, or more important, than the state itself.[44-48] Some measures are, in our view, too reductionistic and obliterate the core nature of frailty. No measure has yet conformed to all the usual requirements of content, construct and criterion validity, and systematic cross-validation. Nevertheless, several useful operational measures exist as first approximations, and allow the field to progress with the prospect of reification of the measures. It must also be acknowledged that much important work on the presentation and/or therapy of frailty (for example, the interventional studies with Tai Chi and other studies carried out under the Frailty and Injuries: Cooperative Studies of Intervention Techniques program[49]) has been achieved without a precise definition being in place. In general, however, greater clarity in the specification of measures of frailty will be needed if authors claims about the characteristics and consequences of frailty are sensibly to be understood.
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6. Conclusion Frailty is a popular and potentially powerful concept that is of especial interest when trying to sort out the risk of adverse health outcomes in older populations. It has intuitive appeal: even though health outcomes are closely related to age, age itself is an insensitive and nonspecific measure of health risk. Although the frailty syndrome may eventually be discovered to have a single critical determinant, we believe this unlikely, and view efforts to translate frailty into, for example, interleukin-6 deficiency or reduced muscle mass as mixing effect with cause. At this point, there is no good empirical test to resolve such a dispute. This paper has reviewed the measurement of frailty from a nominalist perspective, emphasising the complex interaction of body and social systems. We see it as critical that frailty measures point to, if not capture, instability (in the sense of disproportionately large effects from small changes). Precise measurement, nevertheless, has been elusive, but we feel that, to an extent, precision will have to be traded off for comprehensiveness. We see it as important and insightful, for example, that the exact mechanism of achieving a high allostatic load score was less important than the score itself. This suggests that the pathways that underlie frailty are variable and likely to display sensitive dependence on initial conditions. Measures of frailty must be comprehensive and allow for the dynamic interaction of components, by focusing on the state and the manner in which the state was acquired. It is important, therefore, that those seeking to measure frailty embrace its complexity, and not assume it away through specious precision. References
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Correspondence and offprints: Professor Kenneth Rockwood, Division of Geriatric Medicine, Dalhousie University, QEII Health Sciences Centre, 5955 Jubilee Road, Halifax, Nova Scotia, B3H 2E1, Canada. E-mail: rockwood@is.dal.ca

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